scholarly journals Dexamethasone induces sodium-dependant vitamin C transporter in a mouse osteoblastic cell line MC3T3-E1

2001 ◽  
Vol 86 (2) ◽  
pp. 145-149 ◽  
Author(s):  
I. Fujita ◽  
J. Hirano ◽  
N. Itoh ◽  
T. Nakanishi ◽  
K. Tanaka
Keyword(s):  
Vitamin C ◽  
Cell Line ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Culture Conditions ◽  
Osteoblastic Cell ◽  
Prostaglandin E ◽  
Osteoblastic Cell Line ◽  
Cell Functions ◽  
Stimulation Of

The regulation of intracellular ascorbic acid (AsA) levels may be under the control of an AsA-specific membrane transporter. The present study investigates AsA uptake and expression of Na-dependent vitamin C transporter (SVCT) mRNA in the mouse osteoblastic cell line, MC3T3-E1. Among eight compounds tested, dexamethasone (Dex) all-trans retinoic acid, transforming growth factor β, prostaglandin E2 and transferrin significantly (P<0·01, P<0·01, P<0·05 and P<0·01 respectively) stimulated the update of AsA into MC3T3-E1 cells. Among these five, Dex was the most active, inducing mSVCT2 mRNA and the uptake of AsA in a time- and concentration-dependant manner. Dex did not induce mSVCT1 mRNA. These results suggest that the Dex-induced stimulation of AsA incorporation into osteoblastic cells is mediated by the induction of mSVCT2. Since Dex reduced alkaline phosphatase activity in MC3T3-E1 cells in our culture conditions, Dex-induced stimulation of AsA incorporation might not be the result of differentiation. Hormone-regulated changes of SVCT expression may have an important role in cell functions.

Effects of Transforming Growth Factor-β1 on Decorin Expression by Undifferentiated Osteoblastic Cells

1997 ◽  
Vol 3 (S2) ◽  
pp. 187-188
Author(s):  
T. Yamada ◽  
N. Kubushiro ◽  
K. Shigemasa ◽  
T. Ikeda ◽  
M. Takagi
Keyword(s):  
Growth Factor ◽  
Cell Line ◽  
Transforming Growth Factor ◽  
Bone Cells ◽  
Bone Matrix ◽  
Transforming Growth Factor Β ◽  
Osteoblastic Cells ◽  
Osteoblastic Cell ◽  
Experimental Conditions ◽  
Osteoblastic Cell Line

Decorin is the predominant proteoglycan isolated from bone of several animal species. Bone matrix decorin appears to bind transforming growth factor β (TGF-β) and enhances its bioactivity. TGF-β is stored in bone matrix in abundant amounts and modulates the synthesis of bone matrix proteins by osteoblasts. Thus it appears to play a role in regulation of bone formation during the bone remodeling process. The effect of TGF-β on decorin expression in bone cells has been evaluated in murine osteoblastic cells, but the results are divergent depending on the experimental conditions and cell types used. The present study investigated the effect of TGF-βl on the expression of decorin mRNA in two clonal rat osteoblastic cell lines with different stages of differentiation, ROS-C26 (C26) and ROS-C20 (C20); C26 is a potential osteoblast precursor cell line that is also capable of differentiating into muscle cells and adipocytes; C20 is a more differentiated osteoblastic cell line.

scholarly journals Prostaglandin E receptor subtypes in mouse osteoblastic cell line.

Endocrinology ◽  
1996 ◽  
Vol 137 (5) ◽  
pp. 1698-1705 ◽  
Author(s):  
M Suda ◽  
K Tanaka ◽  
K Natsui ◽  
T Usui ◽  
I Tanaka ◽  
...  
Keyword(s):  
Cell Line ◽  
Osteoblastic Cell ◽  
Prostaglandin E ◽  
Receptor Subtypes ◽  
Osteoblastic Cell Line

scholarly journals Production of hydrogen peroxide by transforming growth factor-beta 1 and its involvement in induction of egr-1 in mouse osteoblastic cells.

1994 ◽  
Vol 126 (4) ◽  
pp. 1079-1088 ◽  
Author(s):  
M Ohba ◽  
M Shibanuma ◽  
T Kuroki ◽  
K Nose
Keyword(s):  
Cell Line ◽  
Transforming Growth Factor ◽  
Regulation Of Gene Expression ◽  
Upstream Region ◽  
Osteoblastic Cell ◽  
Transcriptional Level ◽  
Tgf Beta ◽  
Radical Scavengers ◽  
Osteoblastic Cell Line ◽  
Production Of Hydrogen

TGF-beta 1 controls the expression of numerous genes, including early response and cellular matrix genes. However, the signal-transducing mechanism underlying this regulation of gene expression is not fully understood. In this study, we investigated whether redox regulation plays a role in the TGF-beta 1 signal transduction in the mouse osteoblastic cell line (MC3T3-E1). The overall intracellular oxidized state of the cells, when measured using 2',7'-dichlorofluorescin diacetate by laser-scanning confocal microscopy, was increased transiently after the addition of TGF-beta 1. This increase was abolished by the addition of oxygen radical scavengers such as catalase and N-acetylcysteine. In a variant cell line lacking the TGF-beta 1 receptor, the intracellular oxidized state was not modulated by treatment with TGF-beta 1. We then examined the expression of early growth response-1 (egr-1) gene, which is inducible by TGF-beta 1 and H2O2. Radical scavengers inhibited the induction of egr-1 by TGF-beta 1, but not that by 12-O-tetradecanoylphorbol-13 acetate. A nuclear run-on assay indicated that this inhibition was at the transcriptional level. From transient expression experiments using chloramphenicol acetyltransferase gene linked to serially deleted egr-1 gene 5'-upstream region, the CArG element in the 5' flanking region of egr-1 was identified as an essential sequence in the transcriptional activation for both TGF-beta 1 and H2O2 stimulation. These findings suggest that H2O2 acts as a mediator for the TGF-beta 1-induced transcription of egr-1 gene.

scholarly journals Mechanism of Transforming Growth Factor β–induced Inhibition of T Helper Type 1 Differentiation

2002 ◽  
Vol 195 (11) ◽  
pp. 1499-1505 ◽  
Author(s):  
Leonid Gorelik ◽  
Stephanie Constant ◽  
Richard A. Flavell
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Inhibitory Effect ◽  
Interleukin 12 ◽  
T Helper ◽  
Retroviral Transduction ◽  
Cell Functions ◽  
Proliferation And Differentiation ◽  
Direct Inhibitory Effect

Regulation by transforming growth factor (TGF)-β plays an important role in immune homeostasis. TGF-β inhibits T cell functions by blocking both proliferation and differentiation. Here we show that TGF-β blocks Th1 differentiation by inhibiting the expression of T-bet, the apparent masterregulator of T helper (Th)1 differentiation. Restoration of T-bet expression through retroviral transduction of T-bet into developing Th1 cells abrogated the inhibitory effect of TGF-β. In addition, we show that, contrary to prior suggestions, downregulation of interleukin 12 receptor β2 chain is not key to the TGF-β–mediated effect. Furthermore, we show that the direct inhibitory effect of TGF-β on T cells is responsible, at least in part, for the inability of BALB/c mice to mount a Leishmania-specific Th1 response and to clear Leishmanial infection.

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